Intracoronary L-arginine during reperfusion improves endothelial function and reduces infarct size.
Intracoronary L-arginine during reperfusion improves endothelial function and reduces infarct size.
复制标题
再灌注期间冠状动脉内 L-精氨酸可改善内皮功能并减少梗塞面积。
DOI：
10.1152/ajpheart.1992.263.6.h1650
复制
发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Johnston,WE
中科院分区：
文献类型：
--
作者：
Nakanishi,K;Vinten-Johansen,J;Lefer,DJ;Zhao,Z;Fowler3rd,WC;McGee,DS;Johnston,WE
我们验证了在再灌注过程中冠状动脉内给予l -精氨酸（L-Arg），即生理性一氧化氮（NO）前体，可以通过L-Arg NO途径机制减轻缺血后损伤的假设。开胸麻醉犬进行60分钟左冠状动脉前降支闭塞，然后270分钟再灌注。在体外系统再灌注的前120分钟，狗在LAD中接受冠状动脉内10 mM L-Arg （n = 9只狗），冠状动脉内10 mM d -精氨酸（D-Arg, n = 7）或生理盐水（Veh, n = 10）。再灌注270 min后，三组的节段性收缩和舒张功能均明显受损。与Veh组（34.8 +/- 2.4%）相比，L-Arg组（17.7 +/- 3.2%）梗死面积（三苯四唑氯）占危险面积（An/Ar）的百分比显著降低（P < 0.05）；D-Arg逆转了这种心脏保护作用（48.8 +/- 5.2%,P < 0.05, vs. L-Arg, Veh）。心肌髓过氧化物酶活性（中性粒细胞积累指数U/100 mg组织）在l -精氨酸组（0.88 +/- 0.26）显著低于Veh组（2.46 +/- 0.38）（P < 0.05）。此外，l -精氨酸组对内皮依赖性血管扩张剂乙酰胆碱和A23187在离体缺血-再灌注LAD环中的反应显著（P < 0.05）高于其他两组。我们得出结论，在再灌注早期冠脉内输注L-Arg可减少中性粒细胞的积累和梗死面积，并可能通过增加内皮细胞的NO释放或生成来保护内皮功能。
We tested the hypothesis that intracoronary administration of L-arginine (L-Arg), the physiological nitric oxide (NO) precursor, during reperfusion would attenuate postischemic damage by L-Arg NO-pathway mechanisms. Open-chest, anesthetized dogs underwent 60 min of left anterior descending coronary arterial (LAD) occlusion followed by 270 min of reperfusion. Dogs received intracoronary 10 mM L-Arg (n = 9 dogs), intracoronary 10 mM D-arginine (D-Arg, n = 7), or saline vehicle (Veh, n = 10) in the LAD during the first 120 min of reperfusion using an extracorporeal system. After 270 min of reperfusion, segmental systolic and diastolic function were comparably impaired in all three groups. Infarct size (triphenyltetrazolium chloride) expressed as a percentage of the area at risk (An/Ar) was significantly (P < 0.05) reduced in the L-Arg group (17.7 +/- 3.2%) compared with the Veh group (34.8 +/- 2.4%); D-Arg reversed this cardioprotection (48.8 +/- 5.2%, P < 0.05 vs. L-Arg, Veh). Cardiac myeloperoxidase activity, an index of neutrophil accumulation (U/100 mg tissue), was significantly (P < 0.05) lower in the necrotic tissue of the L-Arg group (0.88 +/- 0.26) than in the Veh group (2.46 +/- 0.38). Furthermore, responses to endothelium-dependent vasodilators acetylcholine and A23187 in isolated ischemic-reperfused LAD rings were significantly (P < 0.05) greater in the L-Arg group than in the other two groups. We conclude that intracoronary infusion of L-Arg during the early phase of reperfusion reduced neutrophil accumulation and infarct size and the infusion preserved endothelial function, possibly by increasing NO release or production by the endothelium.